A number of host cell proteins have evolved that inhibit retroviral infection, retroelement mobilization, and/or replication. Examples of such proteins include apoliprotein BmRNA-editing catalytic (APOBEC) polypeptides, tetherin polypeptides and tripartite motif-containing 5 (TRIM5) polypeptides. Certain retroviruses, e.g., HIV, have evolved proteins which antagonize the anti-viral effects of one or more of these proteins. For example, HIV Vpu has been shown to antagonize the anti-viral activity of the tetherin polypeptide, CD317, and HIV Vif has been shown to antagonize the antiviral activity of APOBEC 3G and 3F polypeptides. It has been shown that Vif triggers proteosomal degradation of APOBEC via a physical interaction with APOBEC 3G.
Despite recent advances in HIV research, the World Health Organization (WHO) estimates that currently between 30 and 36 million people worldwide are living with HIV/AIDS and that approximately 2.7 million people were newly infected in the last year (UNAIDS 2008 Report on the global AIDS epidemic). There is a need in the art for methods useful in the treatment and/or prophylaxis of HIV infection.